Pathogenesis of experimental lipid keratopathy: corneal and plasma lipids.

Corneal and plasma lipids were studied in a rabbit model to gain insight into the pathogenesis of secondary lipid keratopathy. Rabbits were divided into four groups in which a high cholesterol diet and corneal suture placement were varied to produce lipid keratopathy. In rabbits with lipid keratopathy, quantitative thin layer chromatography revealed that cholesterol esters comprised most of the deposited lipid, with free cholesterol being deposited as well. The ratio of accumulated cholesterol ester to free cholesterol corresponded closely to the same ratio in hypercholesterolemic plasma total low and very low density lipoprotein (TLDL). Furthermore, gas chromatography showed that the cholesterol ester composition in the corneas with lipid keratopathy resembled that seen in hypercholesterolemic plasma TLDL but was different from the pattern observed in the normal cornea. These studies suggest that the direct source of the deposited cholesterol ester is primarily the plasma TLDL. Since phospholipids and triglycerides did not show a significant increase in the experimental corneas, they are presumably metabolized by the keratocytes after the uptake of TLDL. However, the amount of cholesterol ester carried by the lipoprotein exceeds the capacity of the cell for use and excretion and the lipid accumulates in the cornea.